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Infection and Immunity, April 2006, p. 2402-2414, Vol. 74, No. 4
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.4.2402-2414.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Topical H2 Antagonist Prevents Periodontitis in a Rabbit Model

H. Hasturk,1 A. Kantarci,1 N. Ebrahimi,1 C. Andry,2 M. Holick,3 V. L. Jones,1 and T. E. Van Dyke1*

Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118,1 Department of Pathology, Boston University School of Medicine, Boston, Massachusetts 02118,2 Department of Pharmacology, Boston University School of Medicine, Boston, Massachusetts 021183

Received 12 July 2005/ Returned for modification 13 October 2005/ Accepted 11 January 2006

Cimetidine is a powerful H2 receptor antagonist that eliminates histamine's effects on chemotaxis, phagocytosis, and superoxide anion production by phagocytes. The purpose of this study was to analyze the clinical and histopathological changes associated with experimental periodontitis in rabbits in response to topically applied cimetidine. Experimental periodontitis was induced in 21 New Zealand White rabbits using Porphyromonas gingivalis (109 CFU) topically applied three times a week for a 6-week period to previously ligatured teeth. Topical application of cimetidine in a liposome carrier for the prevention of periodontitis was evaluated in four groups of four animals each: 1, 10, and 100 mg/ml and no treatment (positive control). In addition, there was a vehicle group (n = 3) that received liposome preparation (carrier) only, and two animals with ligature application alone served as negative controls. Periodontal disease was quantified by direct visualization and radiographical evaluation of bone loss on defleshed skulls and by histological analyses of sections stained with hematoxylin-eosin and tartrate-resistant acid phosphatase. In the no-treatment (positive control) and liposome (vehicle) groups, direct visualization and radiological measurements revealed statistically significant bone loss compared to the negative control. Application of cimetidine at all concentrations tested inhibited inflammation and bone loss by >90%. Histological findings revealed that ligated sites of the positive control and vehicle groups showed significant reduction in bone level (P < 0.05) compared to the three cimetidine groups, with a marked decrease in inflammation. The findings of this study provide morphological and histological evidence that topically active cimetidine is a potent inhibitor of P. gingivalis-elicited periodontal inflammation, arresting and/or preventing tissue destruction and influencing cell populations present in the inflammatory cell infiltrate.

* Corresponding author. Mailing address: Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, 100 East Newton Street, Suite 108, Boston, MA 02118. Phone: (617) 638-5227. Fax: (617) 638-4799. E-mail: tvandyke{at}bu.edu.

Editor: J. D. Clements

Infection and Immunity, April 2006, p. 2402-2414, Vol. 74, No. 4
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.4.2402-2414.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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